Synaptic Organization and Plasticity in the Auditory System of the Deaf White Cat

Muniak, Michael A.; Connelly, Catherine J.; Tirko, Natasha N.; O’Neil, Jahn N.; Ryugo, David K.

doi:10.1007/2506_2013_4

Cited by 2 publications

(1 citation statement)

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“…Not even amplification provided by hearing aids is sufficient to provide neural activity levels for optimal transmission particularly at high frequencies (e.g., Takesian, Kotak, Sharma, & Sanes, 2013). However, it is clear that the high level stimulation rates provided by cochlear implants improve or restore integrity of neuroanatomical structures at different stages of the auditory pathway (e.g., Chen, Limb, & Ryugo, 2010;Muniak, Connelly, Tirko, O'Neil, & Ryugo, 2013;O'Neil, Connelly, Limb, & Ryugo, 2011;Ryugo & Limb, 2009). Thus, sensory deprivation causes plastic changes within the brain.…”

Section: Introductionmentioning

confidence: 99%

Structural neuroimaging of the altered brain stemming from pediatric and adolescent hearing loss—Scientific and clinical challenges

Ratnanather

2019

WIREs Mechanisms of Disease

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There has been a spurt in structural neuroimaging studies of the effect of hearing loss on the brain. Specifically, magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI) technologies provide an opportunity to quantify changes in gray and white matter structures at the macroscopic scale. To date, there have been 32 MRI and 23 DTI studies that have analyzed structural differences accruing from pre-or peri-lingual pediatric hearing loss with congenital or early onset etiology and postlingual hearing loss in pre-to-late adolescence. Additionally, there have been 15 prospective clinical structural neuroimaging studies of children and adolescents being evaluated for cochlear implants. The results of the 70 studies are summarized in two figures and three tables. Plastic changes in the brain are seen to be multifocal rather than diffuse, that is, differences are consistent across regions implicated in the hearing, speech and language networks regardless of modes of communication and amplification. Structures in that play an important role in cognition are affected to a lesser extent. A limitation of these studies is the emphasis on volumetric measures and on homogeneous groups of subjects with hearing loss.It is suggested that additional measures of morphometry and connectivity could contribute to a greater understanding of the effect of hearing loss on the brain. Then an interpretation of the observed macroscopic structural differences is given. This is followed by discussion of how structural imaging can be combined with functional imaging to provide biomarkers for longitudinal tracking of amplification.

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Section: Introductionmentioning

confidence: 99%

Structural neuroimaging of the altered brain stemming from pediatric and adolescent hearing loss—Scientific and clinical challenges

Ratnanather

2019

WIREs Mechanisms of Disease

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Central Compensation in Auditory Brainstem after Damaging Noise Exposure

Schrode

Muniak

Kim

et al. 2018

eNeuro

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Noise exposure is one of the most common causes of hearing loss and peripheral damage to the auditory system. A growing literature suggests that the auditory system can compensate for peripheral loss through increased central neural activity. The current study sought to investigate the link between noise exposure, increases in central gain, synaptic reorganization, and auditory function. All axons of the auditory nerve project to the cochlear nucleus, making it a requisite nucleus for sound detection. As the first synapse in the central auditory system, the cochlear nucleus is well positioned to respond plastically to loss of peripheral input. To investigate noise-induced compensation in the central auditory system, we measured auditory brainstem responses (ABRs) and auditory perception and collected tissue from mice exposed to broadband noise. Noise-exposed mice showed elevated ABR thresholds, reduced ABR wave 1 amplitudes, and spiral ganglion neuron loss. Despite peripheral damage, noise-exposed mice were hyperreactive to loud sounds and showed nearly normal behavioral sound detection thresholds. Ratios of late ABR peaks (2–4) relative to the first ABR peak indicated that brainstem pathways were hyperactive in noise-exposed mice, while anatomical analysis indicated there was an imbalance between expression of excitatory and inhibitory proteins in the ventral cochlear nucleus. The results of the current study suggest that a reorganization of excitation and inhibition in the ventral cochlear nucleus may drive hyperactivity in the central auditory system. This increase in central gain can compensate for peripheral loss to restore some aspects of auditory function.

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Synaptic Organization and Plasticity in the Auditory System of the Deaf White Cat

Cited by 2 publications

References 239 publications

Structural neuroimaging of the altered brain stemming from pediatric and adolescent hearing loss—Scientific and clinical challenges

Structural neuroimaging of the altered brain stemming from pediatric and adolescent hearing loss—Scientific and clinical challenges

Central Compensation in Auditory Brainstem after Damaging Noise Exposure

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